lunes, 29 de marzo de 2010

Escherichia albertii in Wild and Domestic Birds


EID Journal Home > Volume 16, Number 4–April 2010

Volume 16, Number 4–April 2010
Research
Escherichia albertii in Wild and Domestic Birds
J. Lindsay Oaks, Thomas E. Besser, Seth T. Walk, David M. Gordon, Kimberlee B. Beckmen, Kathy A. Burek, Gary J. Haldorson, Dan S. Bradway, Lindsey Ouellette, Fred R. Rurangirwa, Margaret A. Davis, Greg Dobbin, and Thomas S. Whittam1
Author affiliations: Washington State University, Pullman, Washington, USA (J.L. Oaks, T.E. Besser, G.J. Haldorson, D.S. Bradway, F.R. Rurangirwa, M.A. Davis); University of Michigan Health System, Ann Arbor, Michigan, USA (S.T. Walk); The Australian National University, Canberra, Australian Capital Territory, Australia (D.M. Gordon); Alaska Department of Fish and Game, Fairbanks, Alaska, USA (K.B. Beckmen); Alaska Veterinary Pathology Services, Eagle River, Alaska, USA (K.A. Burek); Michigan State University, East Lansing, Michigan, USA (L. Ouellette, T.S. Whittam); and University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada (G. Dobbin)


Suggested citation for this article

Abstract
Escherichia albertii has been associated with diarrhea in humans but not with disease or infection in animals. However, in December 2004, E. albertii was found, by biochemical and genetic methods, to be the probable cause of death for redpoll finches (Carduelis flammea) in Alaska. Subsequent investigation found this organism in dead and subclinically infected birds of other species from North America and Australia. Isolates from dead finches in Scotland, previously identified as Escherichia coli O86:K61, also were shown to be E. albertii. Similar to the isolates from humans, E. albertii isolates from birds possessed intimin (eae) and cytolethal distending toxin (cdtB) genes but lacked Shiga toxin (stx) genes. Genetic analysis of eae and cdtB sequences, multilocus sequence typing, and pulsed-field gel electrophoresis patterns showed that the E. albertii strains from birds are heterogeneous but similar to isolates that cause disease in humans.

In late December 2004, deaths of common redpoll finches (Carduelis flammea) were reported around the city of Fairbanks, Alaska, USA, coincident with a prolonged period of extreme cold (below –40°F). The final reported death occurred on February 24. At the beginning of the outbreak, the local at-risk population was estimated to be ≈8,000 redpoll finches, a historic high for the area. Although ≈100 deaths were documented, the actual number is assumed to be considerably higher.

Outbreaks of disease in wild finches (family Fringillidae) have been associated with Salmonella enterica subsp. enterica serotype Typhimurium, Mycoplasma gallisepticum, poxvirus, and Escherichia coli (1–6). Diagnostic investigation into the Alaska outbreak identified Escherichia albertii as the probable cause of death and as a new pathogen for birds. E. albertii had been identified as an enteric pathogen of humans in Asia (7) and, more recently, in Africa and North America (T.S. Whittam and H. Steinsland, unpub. data), but to our knowledge, until this outbreak its presence in animals had not been observed.

We describe the identification and characterization of E. albertii from birds in North America, Europe, and Australia. We show that bacterial isolates from dead finches in Scotland, previously identified as E. coli O86:K61, were actually E. albertii. The genetic diversity of 2 virulence loci (intimin and cytolethal distending toxin) for the bird isolates was compared with characterized human pathotypes. We also determined genetic relatedness among isolates from birds and humans by multilocus sequence typing (MLST) and clonality of multiple isolates from dead or clinically healthy birds by pulsed-field gel electrophoresis (PFGE).

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http://www.cdc.gov/eid/content/16/4/638.htm

Suggested Citation for this Article
Oaks JL, Besser TE, Walk ST, Gordon DM, Beckmen KB, Burek KA, et al. Escherichia albertii in wild and domestic birds. Emerg Infect Dis [serial on the Internet]. 2010 Apr [date cited
]. http://www.cdc.gov/EID/content/16/4/638.htm

DOI: 10.3201/eid1604.090695

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